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. 2015 May 28;21(20):6146–6156. doi: 10.3748/wjg.v21.i20.6146

Table 1.

Androgen receptor expression in esophageal cancer

Ref. No. of patients Male:female Histological type AR Conclusion
Matsuoka et al[74], 1987 NA NA SCC cell line 2.2 fmol/mg Proliferation of KSE-1 cell line is inhibited by estrogen and enhanced by testosterone
Tihan et al[19], 2001 25 21:4 AC (n = 11)SCC (n = 14) 7 males and 1females, 5 EAC and 3 SCC were positive Presence of AR in human esophageal cancer is an impetus for further studies to assess anti-androgen therapy for treatment and or prevention of these tumors.
Yang et al[20], 2001 31 26:5 SCC Cancer tissues: 40.56 ± 18.19 fmol/mg, normal tissues: 7.84 ± 3.21 fmol/mg AR and estrogen receptors have close relationship with the biologic behavior and prognosis of esophageal SCC
Tiffin et al[80], 2003 20 10:10 AC (ND)BE (ND) Very weakly positive in 1 male with EAC and 1 female with BE Androgen receptors are not implicated in BE or AC
Awan et al[17], 2007 23 20:3 AC (n = 18)SCC (n = 5) 16 samples (EAC = 13, SCC = 3) showed positive nuclear staining. AC occurred in 12 males and 1 female, while in SCC 2 males and 1 female AR expressed in the stroma of esophageal AC may induce paracrine effects following stimulation by androgens (including tumor-derived), possibly via FGFs
Nordenstedt, et al[18], 2012 30 20:10 BE (n = 10)Controls (n = 20) All BE cases were negative. Only 1 male control was found AR expressed in squamous esophageal mucosa AR were negative in BE warrants further research to find alternative explanations for the male predominance in BE and EAC

AR: Androgen receptor; EAC: Esophageal adenocarcinoma; SCC: Squamous cell cancer; BE: Barrett’s esophagus; NA: Not applicable; ND: Not described.